The subcutaneous administration of isoproterenol has been shown to stimulate renin secretion and to augment water intake in rats. Both effects are abolished by bilateral nephrectomy. Inasmuch as systemic injections of renin are known to stimulate substantial amounts of drinking in rats, these results collectively suggest that the renin-angiotensin system contributes importantly to thirst during experimental hypotension. However, recently we found that the nephrectomized rats go into hypotensive shock after isoproterenol treatment, which precludes drinking behavior. We now find that drinking can be elicited in these hypotensive animals by intracranial injection of either angiotensin or carbachol, but in both cases a rapid increase in blood pressure is observed to precede the drinking response. In addition, we find that drinking is augmented by intravenous infusion of epinephrine, in doses which raised blood pressure (to 70-80 mm Hg) but did not restore it to normal. Finally, we find that renin prepared from the cortical extracts of rat kidneys, when infused intravenously, elicits significant amounts of drinking only when the induced plasma renin activities are above the physiological range. These results reinforce our previous suggestion that the renin-angiotensin system does not make a direct and substantial contribution to thirst under normal physiological conditions.